Malignant mammary tumor in female dogs: environmental contaminants

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Human papillomavirus (HPV) detection in lip squamous cell carcinoma: correlation with clinical aspects and risk factors

O papilomavírus humano (HPV) está associado a um largo espectro de lesões em humanos e tem sido ligado à carcinogênese oral. O objetivo deste estudo foi investigar a presença do DNA do HPV em pacientes com carcinoma espinocelular de lábio e correlacioná-la com aspectos clínicos e fatores de risco. Foram estudados 33 pacientes com carcinoma espinocelular de lábio. Destes, 30 pacientes foram positivos para o gene da beta-globina humana e então foram testados para o DNA do HPV com uso da reação em cadeia de polimerase em duas etapas (PCR e nPCR) com os oligonucleotídeos iniciadores MY11/MY09 e GP5+/ GP6+. O DNA do HPV foi detectado em 43,33% dos 30 pacientes analisados. Não houve associação com os fatores de risco analisados.

Abnormal cell-cycle expression of the proteins p27, mdm2 and cathepsin B in oral squamous-cell carcinoma infected with human papillomavirus

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Presença do papilomavirus humano em lesões malignas de mucosa oral

O objetivo deste estudo foi investigar a prevalência do papilomavírus humano 6/11 e 16/18 em pacientes, com lesões orais clínicamente diagnosticadas como leucoplasias, atendidas na Faculdade de Odontologia de Araraquara, UNESP, Brasil. Após a inclusão em parafina, os cortes corados com H&E, foram selecionadas 30 biópsias e separadas em 3 grupos: lesões sem displasia (n=10), lesões com diferentes graus de displasia (n=10) e carcinoma espinocelular invasivo(n=10). As lesões que apresentaram displasia epitelial foram classificadas de acordo com os critérios histopatológicos propostos por Van Der Waal. As lesões foram investigadas para a presença de HPV por hibridização in situ com sondas biotiniladas de amplo espectro, 6/11 e 16/18. HPV 16/18 foi detectado em 20% (n=2) das biópsias com displasia severa. A presença de HPV 16/18 em lesões malignas sugere sua importância como fator de risco na carcinogênese oral.

Chromosome 22q a frequent site of allele loss in head and neck carcinoma

Background. Loss of heterozygosity (LOH) correlates with inactivated tumor suppressor genes. LOH at chromosome arm 22q has been found in a variety of human neoplasms, suggesting that this region contains a tumor suppressor gene(s) other than NF2 important to tumorigenesis. The aim of this study was to evaluate the presence of LOH on chromosome 22q11.2-13 and determine whether there was a relationship between loss in this genomic region and tumor histologic parameters, anatomic site, and survival in patients with squamous cell carcinoma of the head and neck (HNSCC).Methods. Fifty matched blood and HNSCC tumor samples taken at the time of surgical treatment were evaluated for LOH by use of four microsatellite markers mapping to 22q11.2-q13. Clinical information was available for all patients. The frequency and distribution of LOH was correlated with clinical (age, sex, use of tobacco and alcohol, site of primary tumor, clinical stage, adjuvant therapy and overall survival) and histologic parameters (histopathologic stage, tumor differentiation).Results. LOH at 22q was found in 19 of 50 (38%) informative tumors. The respective incidence of allelic loss for the patients was as follows: 28% at D22S421, 10% at D22S277, 8% at D22S44S, and 4% at D22S280. No statistical differences were apparent with a mean follow-up of 30 months. Laryngeal tumors showed a higher incidence of LOH compared with oral tumors.Conclusions. These results suggest that the D22S277 locus may be closely linked to a tumor suppressor gene (TSG) and involved in upper aerodigestive tract carcinogenesis. In particular, laryngeal tumors may harbor another putative TSG on 22q11.2-q12.3 that may play a role in aggressive stage III/IV disease. (C) 2000 John Wiley & Sons, Inc.

Cytotoxic constituents of propolis inducing anticancer effects: a review

Objectives Propolis is a honeybee product used extensively in traditional medicine for its antioxidant, anti-inflammatory, immunomodulatory and anticancer effects. Propolis exhibits a broad spectrum of biological activities because it is a complex mixture of natural substances. In this review, the antitumour effects of propolis extracts and its constituents (e. g. flavonoids, terpenes and caffeic acid phenethyl ester) are discussed.Key findings The effect of propolis on experimental carcinogenesis is discussed, as well as its possible mechanisms of action against tumours, involving apoptosis, cell cycle arrest and interference on metabolic pathways. Propolis seems to be efficient against different tumour cells both in vitro and in vivo, which suggests its potential in the development of new anticancer drugs.Summary Propolis extracts may be important economically and would allow a relatively inexpensive cancer treatment. Preclinical investigations are needed to further elucidate the benefits of propolis and its antitumour properties.

Fetotoxicity caused by the interaction between zinc and arsenic in mice

Arsenic is an environmental pollutant that induces congenital malformations in experimental models and can contribute to human birth defects. The environmental exposure to arsenic is relatively small when compared with the doses required to cause teratogenicity in mice and other laboratory animals. In order to study the action of zinc in the arsenic-induced teratogenicity, in the present work mice were either pretreated with zinc and later with arsenic or were treated simultaneously with zinc and arsenic in vivo and in vitro. Following administration of arsenate on gestation day 8, pregnant females were killed on the 17th day of gestation; maternal and fetal data were collected by laparotomy and used to calculate reproductive parameters. Fetuses were analyzed for the presence of external malformation and, after the appropriate processing, visceral and skeletal analyses were accomplished. Conceptuses were exposed in whole embryo culture to arsenicals on gestation day 8 (3-6 somite stage). After a 26 h culture period, morphological development was assessed. Neither pretreatment with zinc nor simultaneous administration of zinc prevented arsenic teratogenicity in these experimental models. (C) 2002 Wiley-Liss, Inc.

In Vivo Models for Measuring Placental Glutatione-S-transferase (GST-P 7-7) Levels: A Suitable Biomarker for Understanding Cancer Pathogenesis

The Glutatione-S-transferases (GSTs) comprise a family of enzymes closely associated with the cell detoxification of xenobiotics. GSTs exist as homo- or heterodimers and have been grouped into at least seven distinct classes. The main function of GSTs is to catalyze the conjugation of reduced glutathione (GSH) to an electrophilic site of a broad range of potentially toxic and carcinogenic compounds, thereby making such compounds less dangerous and enabling their ready-excretion. Placental GST, known as GST-P 7-7, is the main isoform found in normal placental tissue and comprises 67% of the total GST concentration in this tissue. During development, GST-P 7-7 decreases in concentration and is absent in adult tissues. Interestingly, GST-P 7-7 expression has been detected in adult tissues after exposure to carcinogenic agents in several experimental test systems, being considered a reliable biomarker of exposure and susceptibility in early phases of carcinogenesis. In this article, we review a series of studies involving GST-P 7-7 expression as a suitable tool for understanding cancer pathogenesis, especially cancer risk.

Assessment of Female Reproductive Endpoints in Sprague-Dawley Rats Developmentally Exposed to Diuron: Potential Ovary Toxicity

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Aspectos moleculares do câncer tiroideano

A proliferação da célula tiroideana normal é regulada por fatores de crescimento estimuladores e inibidores, que atuam através de seus receptores de membrana e, subseqüentemente, através de transdutores citoplasmáticos. Na glândula normal adulta, o equilíbrio de sinais é tal que a proliferação é mínima, enquanto nas neoplasias o crescimento resulta de um distúrbio irreversível desse equilíbrio. Apesar do número de moléculas envolvidas nesse processo ser grande, apenas um pequeno subgrupo parece estar envolvido na tumorigênese tiroideana. Tais proteínas são codificadas pelos genes RAS, RET, NTRK1 e TP53. O transdutor de sinais ras é ativado por mutações em ponto e constitui uma alteração genética precoce nos tumores com histologia folicular. Os genes dos receptores de crescimento RET e NTRK1 são alterados por rearranjos cromossômicos do tipo translocação ou inversão nos carcinomas papilares e por mutações em ponto nos medulares. As alterações do gene TP53, por sua vez, têm sido observadas em carcinomas tiroideanos pobremente diferenciados e na maioria dos indiferenciados, o que sugere sua participação na progressão dessas lesões. O modelo molecular da carcinogênese tiroideana, embora ainda incompleto, pode fornecer instrumentos importantes para o diagnóstico diferencial e para o desenvolvimento de novas técnicas terapêuticas nesse grupo de neoplasias.

Expression of TERT in precancerous gastric lesions compared to gastric cancer

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

IL-1ra anti-inflammatory cytokine polymorphism is associated with risk of gastric cancer and chronic gastritis in a Brazilian population, but the TNF-beta pro-inflammatory cytokine is not

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gene Mutations in Esophageal Mucosa of Chagas Disease Patients

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Annexin A1 subcellular expression in laryngeal squamous cell carcinoma

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

p53, p16 and Fhit Proteins Expressions in Chronic Esophagitis and Chagas Disease

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)